Evidence map›Paper›PMID 32098256›Full record

Trial reportInternational journal of molecular sciences2020

CLIC1 Protein Accumulates in Circulating Monocyte Membrane during Neurodegeneration.

Valentina Carlini, Ivan Verduci, Francesca Cianci, Gaetano Cannavale, Chiara Fenoglio, Daniela Galimberti, Michele Mazzanti

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. β-Amyloid (Aβ) and Human Cathelicidin LL-37: Two Sides of the Same Coin?International journal of molecular sciences · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Valentina CarliniDipartimento di Bioscienze, Università degli Studi di Milano, 20133 Milano, Italy.
Ivan VerduciDipartimento di Bioscienze, Università degli Studi di Milano, 20133 Milano, Italy.
Francesca CianciDipartimento di Bioscienze, Università degli Studi di Milano, 20133 Milano, Italy.
Gaetano CannavaleDipartimento di Bioscienze, Università degli Studi di Milano, 20133 Milano, Italy.
Chiara FenoglioDipartimento di Fisiopatologia medico-chirurgica e dei trapianti, 20122 Milano, Italy.
Daniela GalimbertiDipartimento di Scienze biomediche, chirurgiche e odontoiatriche, 20122 Milano, Italy.
Michele MazzantiDipartimento di Bioscienze, Università degli Studi di Milano, 20133 Milano, Italy.
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathologies that lead to neurodegeneration in the central nervous system (CNS) represent a major contemporary medical challenge. Neurodegenerative processes, like those that occur in Alzheimer's disease (AD) are progressive, and at the moment, they are unstoppable. Not only is an adequate therapy missing but diagnosis is also extremely complicated. The most reliable method is the measurement of beta amyloid and tau peptides concentration in the cerebrospinal fluid (CSF). However, collecting liquid samples from the CNS is an invasive procedure, thus it is not suitable for a large-scale prevention program. Ideally, blood testing is the most manageable and appropriate diagnostic procedure for a massive population screening. Recently, a few candidates, including proteins or microRNAs present in plasma/serum have been identified. The aim of the present work is to propose the chloride intracellular channel 1 (CLIC1) protein as a potential marker of neurodegenerative processes. CLIC1 protein accumulates in peripheral blood mononuclear cells (PBMCs), and increases drastically when the CNS is in a chronic inflammatory state. In AD patients, both immunolocalization and mRNA quantification are able to show the behavior of CLIC1 during a persistent inflammatory state of the CNS. In particular, confocal microscopy analysis and electrophysiological measurements highlight the significant presence of transmembrane CLIC1 (tmCLIC1) in PBMCs from AD patients. Recent investigations suggest that tmCLIC1 has a very specific role. This provides an opportunity to use blood tests and conventional technologies to discriminate between healthy individuals and patients with ongoing neurodegenerative processes.

Indexed as

AgedAlzheimer DiseaseBiomarkersCell MembraneChloride ChannelsFemaleHumansMaleMiddle AgedMonocytesBiomarkersChloride ChannelsCLIC1 protein, humancell membranechloride channelsCLIC1 proteinmonocytesneurodegenerationPBMC

Identifiers

PMID32098256
PMCPMC7073046
OpenAlexW3007288930

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.